Cultured human fibroblasts are being used to look for genetic receptor and post-receptor defects in insulin resistant patients. Insulin stimulated glucose uptake and Alpha-amino-isobutyric acid (AIB) transport have been examined in cells from an infant with leprechaunism. Fibroblasts from this patient express low affinity insulin receptors. Both of the transport systems appear to function normally in the receptor-mutant cells. The binding of epidermal growth factor (EGF) is markedly reduced in the leprechaun cells. High media glucose levels can partially correct the abnormal insulin binding in the leprechaun cells but not the EGF binding. Other studies with EGF show that in normal fibroblasts, EGF will blunt insulin stimulated activation of glycogen synthase, glucose uptake, and AIB transport. Human growth hormone will also slightly inhibit glucose uptake in these cells, both basally and in the stimulated state.